The process of parturition allows the uterus to contract in a precise manner and the cervix to dilate efficiently, resulting in the safe delivery of the infant. This process, however, is often complicated by deviations from the norm which may result in preterm delivery, or inefficient labor at term with increased infant morbidity and mortality. Primary controlling factors of uterine contractility and cervical dilatation are thought to be the prostaglandins. Studies with human tissues and those from laboratory animals have demonstrated that the amnion and decidua are sources of prostaglandins and oxytocin and that prostaglandins and oxytocin interact to enhance each others secretion. Steroid hormones are thought to be important in regulating the interaction of oxytocin and prostaglandins through extrapolation from other species as well as preliminary evidence using human tissues. There is, however, no data relating oxytocin and prostaglandin secretion in intrauterine tissues in non-human primates. This paracrine interaction is likely controlled through: 1) steroid regulation of intrauterine oxytocin and prostaglandin receptors; 2) the specific secretIon of oxytocin and prostaglandins especially by the amnion and decidua; and 3) a positive feedback loop that leads to increased oxytocin and prostaglandin secretion. Previous studies have demonstrated that there is a gestational age effect on these factors; however, there is no direct evidence that intrauterine oxytocin and prostaglandin dynamics are regulated by steroids. Corticosteroids have been implicated in regulation of prostaglandin secretion from human amnion. The amnion has high affinity glucocorticoid receptors, amnion PGE2 production increases at labor and estradiol enhances decidual prostaglandin production. Oxytocin receptors are present on decidual cells as well as amnion epithelial cells. The decidua is the major source of PGF2alpha, prostaglandin production increases at labor, and estradiol enhances decidual prostaglandin production. The studies outlined in this grant are designed to determine if corticosteroids and oxytocin are important regulators of amnion PGE2 secretion and how estrogen and progesterone affect PGF2alpha release from decidua with and without the influence of added oxytocin. We will collect amnion and decidua from late gestation rhesus macaques and place these cells in culture. We will then manipulate the steroid environment in the cultures to determine how various steroids and combinations of steroids affect prostaglandin secretion. Finally, we will add oxytocin to the culture media to determine if oxytocin can control prostaglandin secretion and how steroids assist this process. Prostaglandins will be measured by specific EIA. The data collected will add to our knowledge of primate parturition for which the rhesus monkey is the primary animal model.